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James, B.

Publications and source records attributed to James, B..

At least 19 recordsLinked to original sources

Careers in Scientific Editing: Results from the 2024 Scientific Editors Network (ScENe) Survey

Funding and publishing scientific research has become increasingly competitive, highlighting a growing need for clear and accurate scientific communication. Scientific editors are professionals who help ensure that grant proposals and research manuscripts meet the standards of funding agencies and peer-reviewed journals while effectively communicating research significance to diverse audiences. However, detailed information characterizing the scientific editing profession is scarce. While some organizations have conducted salary surveys, to our knowledge, no comprehensive survey of the scientific editing field has been conducted. Here, we report findings from a 2024 comprehensive survey of 132 scientific editors. We collected data on demographics and education, career experience and current employment, skills and types of editing, and outcomes and satisfaction. Our data reveal that scientific editors have homogenous demographic characteristics but considerable variability in job titles, employment mechanisms, and career pathways. As the responsibilities of many scientific editors, including supporting proposal development, applying best practices in grantsmanship, and identifying strategies to enhance competitiveness for research funding, overlap with those of research development professionals, our findings provide considerations for further incorporating or defining the role of scientific editors within research development offices. Our results also suggest avenues for scientific editors to start or advance their careers. We anticipate that our results will serve as a foundation for discussions on the future directions of the scientific editing profession as well as areas for future research and professional development.

scientific communication and education↗

In vitro evolution of uropathogenic Escherichia coli to fosfomycin resistance in a 3D cultured human bladder microtissue model

In vitro studies of antimicrobial resistance (AMR) using laboratory growth media produce important, fundamental information. However, their inability to more closely replicate the in vivo environment limits the translational potential of this work. Here, we used a 3D cultured microtissue model which reflects the human bladder microenvironment to select for resistance to fosfomycin in two uropathogenic strains of Escherichia coli, UTI-34 and UTI-59. To assess the clinical relevance of the mutations produced, we screened the observed mutations in the fosfomycin-selected variants against a curated dataset of 14,163 E. coli genomes isolated from urine. The four independent fosfomycin-selected variants of UTI-34 contained diverse mutations, while the mutations in the five independent fosfomycin-selected variants of UTI-59 were more constrained. All variants contained mutations in glpT, uhpT, uhpA and uhpC, which are commonly linked to fosfomycin-resistance in clinical isolates of E. coli. Screening of the mutations against the 14,163 E. coli genomes from urine confirmed that four of these mutations were found as exact matches in the dataset, while other mutation types were confirmed at a regional and gene level. These mutations did not result in any collateral susceptibility or resistance to other antibiotics recommended for the treatment of urinary tract infections. The use of a human 3D microtissue model, which closely replicates the urothelial microenvironment to study AMR during urinary tract infection treatment, could improve the clinical relevance of in vitro AMR studies. This has the potential to provide a better understanding of how AMR is acquired and expressed, and inform new strategies to combat AMR.

microbiology↗

Generation and Characterization of Autotetraploid Sweet Sorghum

Increasing the diversity of biofuel crops can help meet energy demands while also stabilizing the domestic biofuel market. Sorghum bicolor is a promising feedstock for bioethanol production due to its sugar accumulation and storage in the stem in addition to its cellulosic biomass. Sorghum also exhibits high tolerance to abiotic stresses like extreme temperatures and drought. However, sorghums sugar production falls short when compared to current bioethanol feedstocks like maize and sugarcane. Therefore, to improve sorghum for the bioethanol market, an autotetraploid sorghum line was induced using colchicine treatments to increase cell size for greater sugar production and storage. Induced autotetraploid sorghum lines were validated with flow cytometry and screened using stomatal prints to detect larger stomatal cells. Two separate autotetraploid sorghum lines that were derived from the same M1 plant were characterized and evaluated for sugar production in a two-year field trial. The two autotetraploid lines displayed equal or improved performance when compared to their diploid equivalents for multiple juicing traits. Altogether, the data illustrate sorghums tolerance for autopolyploidy induction in an inbred background and suggest an opportunity for further improvements through progressive heterosis. SIGNIFICANCE STATEMENTPolyploidy has played a significant role in the improvement of some crop species. The characterization of a novel autotetraploid sweet sorghum line demonstrates the potential of increased sugar production in polyploids for biofuel applications.

plant biology↗

Transposable element disruption of a second thyroglobulin-like gene confers Vip3Aa resistance in Helicoverpa armigera

BackgroundThe cotton bollworm Helicoverpa armigera is a major global pest controlled by genetically engineered crops expressing Bacillus thuringiensis (Bt) toxins, including Vip3Aa. While Vip3Aa is widely deployed, the genetic basis of resistance remains poorly understood. Previous work identified disruption of a thyroglobulin-like gene (HaVipR1) as one mechanism of resistance, suggesting additional loci may be involved. ResultsUsing linkage analysis, transcriptomics, long-read sequencing, and CRISPR-Cas9 gene editing, we identify a second thyroglobulin-like gene, HaVipR2, as a novel mediator of Vip3Aa resistance. Resistance in a field-derived H. armigera line was shown to be monogenic, recessive, and autosomal, mapping to chromosome 29. Long-read sequencing revealed a [~]16 kb transposable element insertion disrupting HaVipR2, which was undetectable using standard short-read approaches. CRISPR-Cas9 knockout of HaVipR2 conferred >900-fold resistance, confirming its causal role. Comparative analyses show that HaVipR1 and HaVipR2 share conserved domain architecture, indicating that thyroglobulin-domain proteins represent a recurrent target of resistance evolution. ConclusionsOur findings establish thyroglobulin-domain proteins as a new class of Bt resistance genes in Lepidoptera and demonstrate that transposable element insertions can drive adaptive resistance while evading detection by conventional methods. These results highlight the importance of long-read sequencing and accurate genome annotation for resistance monitoring and provide new insights into the molecular basis and evolution of Vip3Aa resistance.

genomics↗

Transcription Factor Subtype Governs Response and Resistance to DLL3-Directed T-Cell Engagement in Small Cell Lung Cancer

Although small cell lung cancer (SCLC) comprises transcription factor (TF)-defined molecular subtypes (ASCL1, NEUROD1, POU2F3), the extent to which these subtypes predict response to clinically effective therapy in patients--and whether therapy can select for subtype switching--remains unknown. The recent approval of the DLL3xCD3 bispecific T-cell engager tarlatamab represents one of the first meaningful advances in relapsed small cell lung cancer (SCLC) in decades, yet responses remain heterogeneous and resistance is inevitable. Here, we inferred SCLC gene expression from circulating chromatin in prospectively collected patient plasma (46 patients; 167 samples), enabling interrogation of response and acquired resistance to tarlatamab. Parallel development of the first immunocompetent syngeneic mouse model to study tarlatamab response and resistance enabled functional validation. Across species, findings converged on a central principle: TF subtype governs both initial response and acquired resistance. Therapeutic response was significantly associated with ASCL1-subtype tumors, whereas NEUROD1-subtype tumors exhibited inferior responses and POU2F3-subtype tumors were uniformly resistant, consistent with DLL3 being a direct ASCL1 transcriptional target and most highly expressed in ASCL1-positive tumors. Strikingly, one mode of acquired resistance revealed therapeutic selection for a NEUROD1-high state with concomitant DLL3 downregulation. Other resistant tumors exhibited enrichment of regulatory and exhausted T-cell programs, highlighting tarlatamabs dual-targeting mechanism of action. Together, these results reveal that tarlatamab exerts selective pressure against ASCL1-driven lineages, facilitating resistance through loss of an antigen intrinsically linked to that state. These findings underscore the clinical relevance of TF-defined molecular subtypes in human SCLC. More broadly, they highlight the power of integrating longitudinal in vivo plasma transcriptional profiling from patient plasma with functional mouse modeling to uncover clinical and biological mechanisms of response and resistance to cell-surface-targeted therapies.

cancer biology↗

Integrated inference of cancer gene expression from cell-free plasma chromatin

Gene expression is a defining determinant of tumor identity, behavior, and therapeutic response, yet remains challenging to measure noninvasively. Here, we introduce APEX (Associating Plasma Epigenomic features with eXpression), a framework for inferring expression from circulating cell-free chromatin. Trained on [~]270,000 gene-sample pairs from matched tumor RNA-seq and plasma cfChIP-seq across multiple cancers and validated on >15 unseen cancer subtypes, APEX accurately infers cancer gene expression across a range of tumor fractions and outperforms existing plasma-based approaches by integrating positional histone mark and DNA fragmentation patterns across promoters and gene bodies. Using plasma alone, APEX enables classification of prognostically relevant basal and classical pancreatic cancer subtypes and identifies plasma-inferred NECTIN4 expression as a biomarker of response to enfortumab vedotin in metastatic bladder cancer. Together, these findings establish APEX as a biopsy-free approach for profiling tumor transcriptional states and extend liquid biopsy beyond genomic alterations to clinically relevant gene expression programs.

genomics↗

Type 2 Diabetes and Obesity Alter Exercise Training-Induced Transcriptional Adaptations to Subcutaneous White Adipose Tissue

White adipose tissue (WAT) dysfunction contributes to obesity-associated metabolic disease and type 2 diabetes (T2D). Rodent studies have demonstrated that exercise training improves WAT function, but molecular studies investigating exercise training effects on WAT in humans have been limited, particularly in the context of metabolic disease. Here, we defined the subcutaneous WAT (scWAT) transcriptome in middle-aged adults (10 male, 19 female) that were classified by lower BMI (<27 kg/m2), higher BMI ([&ge;]27 kg/m2), and T2D status before and after a 10-week endurance exercise regimen. At baseline, 624 genes were significantly upregulated and 112 genes downregulated in the scWAT from higher BMI participants compared to lower BMI. There was a spectrum of pathway dysregulation in scWAT in higher BMI individuals, ranging from increased markers of extracellular matrix (ECM) deposition and inflammation to decreased circadian rhythm gene expression. In people with T2D, there were additional transcriptomic differences such as translation-related pathways, selenoamino acid metabolism, and proteoglycans. Exercise training had robust effects on the transcriptome regardless of metabolic status, and notably, for the high BMI and T2D groups, training reversed several of the detrimental gene expression patterns in a cell-type-specific manner. These beneficial exercise-induced transcriptomic adaptations significantly correlated with lower levels of free fatty acids and blood pressure, particularly in participants with higher BMI and T2D. By integrating our exercise training-modulated genes with GWAS meta-analysis of physical activity, genes influenced by exercise training in the higher BMI group showed a significant enrichment in genetic associations of exercise traits in the population. A circadian rhythm-related transcription factor NR1D1 was enriched in enhancers linked with both the exercise differentially expressed genes (DEGs) and GWAS signals, suggesting a link between the circadian rhythm and training-induced adaptations. These findings demonstrate that obesity and T2D result in marked, progressive alterations in cell-type specific gene transcription in scWAT, while endurance exercise training reverses many of the metabolic disease-associated adaptations. Identification of novel molecular pathways regulated by exercise training can lead to therapeutic targets for obesity and metabolic disease.

molecular biology↗

Stage-resolved gene regulatory network analysis reveals developmental reprogramming and genes with robust stem-preferred expression in sorghum

BackgroundSorghum bicolor is a deep-rooted, heat- and drought-tolerant crop that thrives on marginal lands and is increasingly valued for its applications in biofuel, bioenergy, and biopolymer production. The sorghum stem, which can reach 4-5 meters in length, serves as the primary reservoir of both lignocellulosic biomass and soluble sugars, making it a promising bioenergy feedstock. Although recent advances in genetic, genomic, and transcriptomic resources have improved our understanding of sorghum biology, comprehensive genome-wide analyses of functional dynamics across diverse organ types and developmental stages remain limited. In particular, candidate genes with stem preferred expression pattern or their associated cis-regulatory elements, which may program key stem-related functions and enable organ- or tissue-specific engineering, have not yet been identified. ResultsTo address these gaps, we reanalyzed a published RNA-seq dataset to identify genes with organ-preferential expression and to infer representative organ functions across major developmental stages. Our analysis revealed that the sorghum stem exhibits distinct temporal functional signatures, which correlate with the developmental dynamics of stem-specific genes and their associated regulatory elements. We further identified a set of genes with ubiquitous stem-specific expression across diverse sorghum genotypes, suggesting their universal importance and broad potential for genetic engineering applications. Among them, SbTALE03 and SbTALE04 emerged as stem hub transcription factors (TF). Both genes were empirically validated for their stem specificity across stages. Gene regulatory network analysis further indicated that these TFs participate in stage-specific transcriptional programs that maintain and regulate stem development. ConclusionsThis study presents a genome-wide analysis of organ-specific gene expression, functions, and regulatory networks in sorghum, with a focus on genes preferentially-expressed in stems and their promoter motifs. We identified a set of core stem-specific genes with ubiquitous expression across genotypes and developmental stages, including two experimentally validated transcription factors with potential roles in stem development. These findings offer valuable candidates for further functional characterization and genetic engineering aimed at improving sorghum stem biomass and composition.

plant biology↗

Whole-brain, all-optical interrogation of neuronal dynamics underlying gut interoception in zebrafish

Internal signals from the body and external signals from the environment are processed by brain-wide circuits to guide behavior. However, the complete brain-wide circuit activity underlying interoception--the perception of bodily signals--and its interactions with sensorimotor circuits remain unclear due to technical barriers to accessing whole-brain activity at the cellular level during organ physiology perturbations. We developed an all-optical system for whole-brain neuronal imaging in behaving larval zebrafish during optical uncaging of gut-targeted nutrients and visuo-motor stimulation. Widespread neural activity throughout the brain encoded nutrient delivery, unfolding on multiple timescales across many specific peripheral and central regions. Evoked activity depended on delivery location and occurred with amino acids and D-glucose, but not L-glucose. Many gut-sensitive neurons also responded to swimming and visual stimuli, with brainstem areas primarily integrating gut and motor signals and midbrain regions integrating gut and visual signals. This platform links body-brain communication studies to brain-wide neural computation in awake, behaving vertebrates.

neuroscience↗

Interleukin-6 elevates thrombosis via pro-coagulant phospholipids from platelet 12-lipoxygenase in rheumatoid arthritis.

BackgroundRheumatoid arthritis (RA) is associated with significantly higher thrombotic risk, which is not yet mechanistically understood. Here, the role of pro-coagulant membranes of platelets and blood cells in driving thrombosis, and their regulation by inflammation was determined using human cohorts and genetically-modified mice. MethodsAntigen-induced arthritis (AIA) was induced in WT, Il27ra-/-, Il6ra-/-, Alox12-/- and Alox15-/- mice. Coagulation and inflammatory markers were measured in plasma. Lipidomics was performed on blood cells and synovium analyzing pro-coagulant enzymatically-oxidized phospholipids (eoxPL) and oxylipins. Two human RA patient cohorts were characterized for eoxPL generation in blood cells, and chronic immune response to eoxPL in vivo. ResultsAIA induction significantly elevated plasma thrombin-antithrombin (TAT) complexes, serum amyloid A (SAA), and eoxPL in blood cells and platelets. Elevations in TATs, SAA and eoxPL were suppressed by genetic deletion of IL-6Ra, while platelet Alox12 deletion prevented TAT and eoxPL increases. This indicates a direct role for IL-6 in elevating thrombosis via upregulation of platelet eoxPL. In contrast, leukocyte Alox15 deletion did not impact TATs or eoxPL. Deletion of either LOX isoform worsened AIA joint pathology. Synovial tissue demonstrated raised eoxPL, but exclusively from Alox15, indicating leukocyte origin. Thus, both LOX isoforms contribute to AIA, but through different mechanisms. In human RA, platelet counts, and plasma TATs were elevated, and plasma had significantly elevated IgG against eoxPL, indicating patients experience chronic exposure to the lipids in vivo. ConclusionsPlatelet-derived pro-coagulant eoxPL are elevated in human and murine arthritis along with higher coagulation markers. In mice, this was mediated by the IL-6/Alox12 axis and directly responsible for the higher thrombotic risk. IL-6 plays a central role in driving platelet activation in RA, with the pro-coagulant lipid membrane representing a novel target. Reducing inflammation using DMARDs, particularly targeting IL-6 may reduce platelet pro-coagulant activity and thrombosis risk in RA.

pharmacology and toxicology↗

Synergistic RAS-MAPK and AKT Activation in MYC-Driven Tumors via Adjacent PVT1 Rearrangements

MYC-driven (MYC+) cancers are aggressive and often fatal. MYC dysregulation is a key event in these cancers, but overexpression of MYC alone is not always enough to cause cancer. Plasmocytoma Variant Translocation 1 (PVT1), a long non-coding RNA (lncRNA) adjacent to MYC on chromosome 8 is a rearrangement hotspot in many MYC+ cancers. In addition to being co-amplified with MYC, the genomic rearrangement at PVT1 involves translocation, which has had obscure functional consequences. We report that translocation at the PVT1 locus cause asymmetric enrichment of 5-PVT1 and loss of 3-PVT1. Despite being classified as a non-coding RNA, the retained 5 region of PVT1 generates a circular RNA (CircPVT1) that codes for the novel peptide we call Firefox (FFX). FFX augments AKT signaling and synergistically activates MYC and mTORC1 in these cells. Further, the 3 end of PVT1, which is lost during the translocation, codes for a tumor-suppressing micropeptide we named as Honeybadger (HNB). We demonstrate that HNB interacts with KRAS and disrupts the activation of KRAS effectors. Loss of HNB leads to activation of RAS/MAPK signaling pathway, and enhances MYC stability by promoting phosphorylation of MYC at Ser62. These findings identify PVT1 as a critical node that synchronizes MYC, AKT, and RAS-MAPK activities in cancer. Our study thus identifies a key mechanism by which rearrangements at the PVT1 locus activate additional oncogenic pathways that synergize with MYC to exacerbate the aggressiveness of MYC+ cancers. This newfound understanding explains the poor prognosis associated with MYC+ cancers and offers potential therapeutic targets that could be leveraged in treatment strategies for these cancers.

cancer biology↗

Identification of a novel resistance gene which provides insight into Vip3Aa mode of action in Helicoverpa armigera

The global reliance on Bacillus thuringiensis (Bt) proteins for controlling lepidopteran pests in cotton, corn, and soybean crops underscores the critical need to understand resistance mechanisms. Vip3Aa, one of the most widely deployed and currently effective Bt proteins in genetically modified crops, plays a pivotal role in pest management. This study identifies the molecular basis of Vip3Aa resistance in Australian Helicoverpa armigera through genetic crosses, and integrated genomic and transcriptomic analyses. We identified a previously uncharacterized gene, LOC110373801 (designated HaVipR1), as a crucial determinant of Vip3Aa resistance in two field-derived resistant lines. Functional validation using CRISPR-Cas9 knockout in susceptible lines confirmed the genes role in conferring resistance. Despite extensive laboratory selection of Vip3Aa-resistant colonies in Lepidoptera, the biochemical mechanisms underlying resistance have remained elusive. Our research demonstrates that HaVipR1-mediated resistance operates independently of known resistance genes, including midgut-specific chitin synthase and the transcription factor SfMyb. The identification of HaVipR1 offers further insights into the Vip3Aa mechanism of action. This discovery is vital for devising strategies to counteract resistance and sustain the efficacy of Bt crops. Future research should focus on elucidating the biochemical pathways involving HaVipR1 and investigating its interactions with other resistance mechanisms. Our findings underscore the utility of analysing field-derived resistant lines in providing biologically relevant insights and stress the necessity for comprehensive management strategies to maintain agricultural productivity. Significance StatementThis is the first identification of a specific gene in Helicoverpa armigera which mediates resistance to the Bacillus thuringiensis (Bt) protein Vip3Aa. We identify that this gene is disrupted in two different ways in separate field-derived resistant lines, one being a large transposable element insertion in the first intron of the HaVipR1 gene, confirmed using long-read sequencing. Disruption of this gene using CRISPR-Cas9 knockout in a susceptible H. armigera line confers Vip3A resistance. The identification of a specific gene is important for molecular monitoring and management of H. armigera as well as other global pests of concern like Spodoptera frugiperda. These findings also offer insights for researchers aiming to understand how Vip3Aa functions, as the action pathway remains unclear.

genomics↗

A heterogeneous population code at the first synapse of vision

Vision begins when photoreceptors convert light fluctuations into temporal patterns of glutamate release that drive the retinal network. The input-output relation at this first stage has not been systematically measured in vivo so it is not known how it operates across a photoreceptor population. Using kHz-rate glutamate imaging in zebrafish, we find that individual red cones encode visual stimuli with high reliability and time-precision, but routinely vary in sensitivity to luminance, contrast, and frequency across the population. Variations in input-output relations are generated by feedback from the horizontal cell network that effectively decorrelate feature representation. A model capturing how zebrafish sample their visual environment indicates that this heterogeneity expands the dynamic range of the retina to improve the coding of natural scenes. Moreover, we find that different kinetic release components are used to encode distinct stimulus features in parallel: sustained release linearly encodes low amplitude light and dark contrasts, but transient release encodes large amplitude dark contrasts. Together, this study reveals an unprecedented degree of functional heterogeneity within same-type photoreceptors and illustrates how separation of different visual features begins in the first synapse in vision.

neuroscience↗

Engineered 3D Immuno-Glial-Neurovascular Human Brain Model

Patient-specific, human-based cellular models integrating a biomimetic blood-brain barrier (BBB), immune, and myelinated neuron components are critically needed to enable accelerated, translationally relevant discovery of neurological disease mechanisms and interventions. By engineering a novel brain-mimicking 3D hydrogel and co-culturing all six major brain cell types derived from patient iPSCs, we have constructed, characterized, and utilized a multicellular integrated brain (miBrain) immuno-glial-neurovascular model with in vivo-like hallmarks inclusive of neuronal activity, functional connectivity, barrier function, myelin-producing oligodendrocyte engagement with neurons, multicellular interactions, and transcriptomic profiles. We implemented the model to study Alzheimers Disease pathologies associated with APOE4 genetic risk. APOE4 miBrains differentially exhibit amyloid aggregation, tau phosphorylation, and astrocytic GFAP. Unlike the co-emergent fate specification of glia and neurons in organoids, miBrains integrate independently differentiated cell types, a feature we harnessed to identify that APOE4 in astrocytes promotes neuronal tau pathogenesis and dysregulation through crosstalk with microglia.

neuroscience↗

The stem cell-type transcriptome of bioenergy sorghum reveals the spatial regulation of secondary cell wall networks

Bioenergy sorghum is a low-input, drought-resilient, deep-rooting annual crop that has high biomass yield potential enabling the sustainable production of biofuels, biopower, and bioproducts. Bioenergy sorghums 4-5 m stems account for [~]80% of the harvested biomass. Stems accumulate high levels of sucrose that could be used to synthesize bioethanol and useful biopolymers if information about stem cell-type gene expression and regulation was available to enable engineering. To obtain this information, Laser Capture Microdissection (LCM) was used to isolate and collect transcriptome profiles from five major cell types that are present in stems of the sweet sorghum Wray. Transcriptome analysis identified genes with cell-type specific and cell-preferred expression patterns that reflect the distinct metabolic, transport, and regulatory functions of each cell type. Analysis of cell-type specific gene regulatory networks (GRNs) revealed that unique TF families contribute to distinct regulatory landscapes, where regulation is organized through various modes and identifiable network motifs. Cell-specific transcriptome data was combined with a stem developmental transcriptome dataset to identify the GRN that differentially activates the secondary cell wall (SCW) formation in stem xylem sclerenchyma and epidermal cells. The cell-type transcriptomic dataset provides a valuable source of information about the function of sorghum stem cell types and GRNs that will enable the engineering of bioenergy sorghum stems.

plant biology↗

The lung employs an intrinsic surfactant-mediated inflammatory response for viral defense

Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) causes an acute respiratory distress syndrome (ARDS) that resembles surfactant deficient RDS. Using a novel multi-cell type, human induced pluripotent stem cell (hiPSC)-derived lung organoid (LO) system, validated against primary lung cells, we found that inflammatory cytokine/chemokine production and interferon (IFN) responses are dynamically regulated autonomously within the lung following SARS-CoV-2 infection, an intrinsic defense mechanism mediated by surfactant proteins (SP). Single cell RNA sequencing revealed broad infectability of most lung cell types through canonical (ACE2) and non-canonical (endocytotic) viral entry routes. SARS-CoV-2 triggers rapid apoptosis, impairing viral dissemination. In the absence of surfactant protein B (SP-B), resistance to infection was impaired and cytokine/chemokine production and IFN responses were modulated. Exogenous surfactant, recombinant SP-B, or genomic correction of the SP-B deletion restored resistance to SARS-CoV-2 and improved viability.

immunology↗

Spatio-temporal monitoring of lake fish spawning activity using environmental DNA metabarcoding

Determining the timing and location of fish reproductive events is crucial for the implementation of correct management and conservation schemes. Conventional methods used to monitor these events are often unable to assess the spawning activity directly or can be invasive and therefore problematic. This is especially the case when threatened fish populations are the study subject, such as the Arctic charr (Salvelinus alpinus L.) populations in Windermere (Cumbria, UK). Arctic charr populations have been studied in this lake since the 1940s, and the locations and characteristics of spawning grounds have been described in detail using techniques such as hydroacoustics, as well as physical and visual surveys of the lake bottom. Here, in conjunction with established netting surveys, we added an environmental DNA (eDNA) metabarcoding approach to assess the spatial distribution of Arctic charr in the lake throughout the year to test whether this tool could allow us to identify spawning locations and activity. Sampling was carried out between October 2017 and July 2018 at three locations in the lake, covering putative and known spawning sites. eDNA metabarcoding provided accurate spatial and temporal characterisation of Arctic charr spawning events. Peaks of Arctic charr read counts from eDNA metabarcoding were observed during the spawning season and at specific locations of both putative and known spawning sites. Net catches of mature Arctic charr individuals confirmed the association between the Arctic charr spawning activity and the peaks of eDNA metabarcoding read counts. This study demonstrates the ability of eDNA metabarcoding to effectively and efficiently characterize the spatial and temporal nature of fish spawning in lentic systems.

molecular biology↗

A brainstem integrator for self-localization and positional homeostasis

To accurately track self-location, animals need to integrate their movements through space. In amniotes, representations of self-location have been found in regions such as the hippocampus. It is unknown whether more ancient brain regions contain such representations and by which pathways they may drive locomotion. Fish displaced by water currents must prevent uncontrolled drift to potentially dangerous areas. We found that larval zebrafish track such movements and can later swim back to their earlier location. Whole-brain functional imaging revealed the circuit enabling this process of positional homeostasis. Position-encoding brainstem neurons integrate optic flow, then bias future swimming to correct for past displacements by modulating inferior olive and cerebellar activity. Manipulation of position-encoding or olivary neurons abolished positional homeostasis or evoked behavior as if animals had experienced positional shifts. These results reveal a multiregional hindbrain circuit in vertebrates for optic flow integration, memory of self-location, and its neural pathway to behavior.

neuroscience↗